Pressemitteilungen

Limited places available - Application Deadline: June 30, 2018

Application form Symposium 2018

Submit your application by email: GRK2162-symposium(at)fau.de

Confirmed Speakers:

• Keynote: Fred H. Gage (Salk Institute, USA)
• André Fischer (DZNE, Germany)
• Hongjun Song (UPenn, USA)
• Guo-Li Ming (UPenn, USA)
• Francesca Peri (EMBL, Germany)
• Sebastian Jessberger (UZH, Switzerland)
• Verdon Taylor (University of Basel, Switzerland)
• Illeana Hanganu-Opatz (UKE, Germany)
• Victor Borrell (CSIC, Spain)
• Tobias Böckers (University of Ulm, Germany)
• Melanie Meyer-Lühmann (University of Freiburg, Germany)
• Denis Jabaudon (Université de Genève, Switzerland)
• Leda Dimou (University of Ulm, Germany)
• Klaus Armin Nave (MPI für Experimentelle Medizin, Germany)
• Hans van Bokhoven (Radboud UMC, The Netherlands)
• Gaia Novarino (IST, Austria)

Hereditary spastic paraplegia is a rare motor neuron disease characterized by progressive gait impairment. Cases that are caused by autosomal-recessive mutations in the gene SPG11 show a complex phenotype with additional symptoms including cognitive impairment due to neurodevelopmental abnormalities. In the Department of Stem Cell Biology (Head: Prof. Dr. Beate Winner), different patient-specific neuronal models of SPG11-linked neurodegeneration have been successfully established to provide more insight into disease mechanisms and potential cures.

These advancements have been honored at the 2018 symposium of the Tom Wahlig Foundation in Berlin. Tatyana Pismenyuk (graduate student of the department) received a prize for her poster presentation "Rescue of neurodevelopmental and neurodegenerative phenotypes in SPG11 by tideglusib". In collaboration with Dr. Martin Regensburger (clinician scientist of the department), she also received funding for an in vitro study on the role of adipocytokines in SPG11 hereditary spastic paraplegia.

More information: beate.winner(at)uk-erlangen.de

Link to Tom Wahlig Foundation: http://www.hsp-info.de/en/researchers/project_reports.htm

Neurodegeneration in Parkinson’s disease has been linked to aggregation of the presynaptic protein alpha-synuclein. Specifically, the oligomeric species of alpha-synuclein were suggested to mediate neurotoxicity. Using the adult neurogenic niche as a disease model of alpha-synucleinopathy, we demonstrate a dendrite phenotype of newborn neurons in alpha-synuclein transgenic mice, which is more pronounced when using an oligomer-prone alpha-synuclein mutant. Thus, the adult neurogenic niche serves as a model to improve the understanding of early disease mechanisms in Parkinson’s disease.

We wrote a review article on the emerging theme of the role of T cells for neurodegenerative diseases.

Contacts between endosomes and the endoplasmic reticulum (ER) promote endosomal tubule fission, but the mechanisms involved and consequences of tubule fission failure are incompletely understood. We found that interaction between the microtubule-severing enzyme spastin and the ESCRT protein IST1 at ER–endosome contacts drives endosomal tubule fission.